Brij G. Goel

Re-entrant beats induced in the ventricle during coronary occlusion☆

Abstract Re-entrant beats were induced in dog ventricles during occlusion of the anterior descending artery. When the excitability and conductivity were markedly depressed in the ischemic area, premature responses were slowly propagated through the ischemic area and frequently emerged to reexcite the surrounding normal tissue. The results indicate that slow conduction of the impulse through the ischemic area permitted the normal area to recover its excitability in time to accept the re-entrant impulse emerging from the ischemic area. Such re-entrant activity was established intermittently or repetitively, resulting in isolated extrasystoles or sustained tachycardia in the ventricle. The study supports the concept that some ectopic beats occurring in the ventricle with myocardial infarction are due to re-entrant circuits established between normal and ischemic areas as a result of the difference in excitability and conductivity.

Atrial Ectopic Activity Associated with Sinus Bradycardia

Five cases of atrial ectopic activity associated with sinus bradycardia are reported. The ectopic activity was abolished in all cases when the sinus rate was increased spontaneously or by atropine. The report demonstrated that the incidence of ectopic activity increases in the atrium at the slower basic rates as it does in the ventricle. It was emphasized that atrial ectopic activity associated with sinus bradycardia should be treated by atropine or by rapid pacing of the atrium because atrial premature beats have the potential of inducing more serious atrial tachyarrhythmias. The possible role of the vagus nerves in facilitating the induction of atrial tachyarrhythmias was discussed, and it was suggested that atropine may have an added benefit of reducing the likelihood of development of atrial tachyarrhythmias.

Effect of procainamide on fibrillation threshold of normal and ischemic ventricles

Abstract The effect of procainamide on ventricular fibrillation threshold was studied in anesthetized open chest hearts in 12 dogs without coronary occlusion and in 11 dogs during acute coronary occlusion. The minimal current required to induce ventricular fibrillation was determined by delivering a train of rapid rectangular pulses (100/sec) to the ventricle during its vulnerable period. Procainamide was administered as a single intravenous injection in a dose of 10 to 20 mg/kg body weight. Blood levels of the drug reached their peak immediately, fell to therapeutic levels (5 to 10 μg/ml) within about 30 minutes and then remained at those levels up to 80 minutes after the injection. The effect of procainamide on the fibrillation threshold correlated with procainamide blood levels. The increase, peak level and decrease in blood concentration paralleled changes in fibrillation threshold. Procainamide at therapeutic blood levels increased the mean fibrillation threshold from the control value of 16 to 30 ma (88 percent increase) in the normal ventricles. The effect was less pronounced during acute coronary occlusion, and the mean fibrillation threshold increased from 8 to 13 ma (63 percent increase) at therapeutic procainamide blood levels. In addition, procainamide failed to produce complete reversion of the decreased fibrillation threshold to the normal value during acute myocardial ischemia.

Effect of procainamide and lidocaine on ventricular automaticity and reentry during acute coronary occlusion

Abstract A model was developed to study ventricular automaticity and reentry in the heart of open chest dogs during myocardlal ischemia. Atrioventricular (A-V) block and the resultant idioventricular rhythm were induced by surgical destruction of the His bundle, and acute myocardial ischemia was produced by ligation of the left anterior descending coronary artery. The ventricle was paced by basic stimuli, and one or two premature beats were introduced at various coupling Intervals after the 10th basic beat. Two different types of response to these premature beats could be observed: (1) rapidly repetitive beats or fibrillation due to reentry after early premature beats, and (2) the appearance of escape beats from idioventricular automatic fibers after late premature beats. With this model of ventricular reentry and automaticity, the effect of procainamide (group I antiarrhythmic agent) was studied in 12 dogs, and that of lidocaine (group II) in 13 dogs. Both procainamide and lidocaine were effective in decreasing automaticity since they significantly increased postextrasystolic escape intervals of idloventricular beats. Although procainamide failed to abolish the reentrant beats induced by early premature beats in all 12 dogs, lidocaine abolished these beats in 10 of 13 dogs. The results indicate that lidocaine is much more effective than procainamide in preventing ventricular reentrant activity induced by early premature beats.

Experimental model for study of “sudden death” from ventricular fibrillation or asystole

Sudden death as a result of cardiac arrhythmias can be induced in swine by combining precordial X-irradiation and an atherogenic diet. Hypothyroidism was not essential to the rapid induction of disease. We monitored the electrical activity of the heart during the terminal episode in 18 swine; 13 electrocardiograms showed ventricular fibrillation and 5 showed ventricular asystole. All 18 animals had advanced coronary atherosclerosis, and 14 had anatomically demonstrable myocardial infarcts. In a correlated separate experiment, ventricular fibrillation threshold was significantly lower in atherosclerotic swine. Infusion of lidocaine increased the fibrillation threshold 4-fold in these animals. This animal model appears to be useful for other investigations related to cardiac arrhythmias.

A-V conduction in hyper- and hypothyroid dogs☆

Abstract Dogs were made hyper- or hypothyroid by daily feeding of thyroid powder or intraperitoneal injection of 131 I, and serum thyroxine levels were determined to confirm their abnormal thyroid states. Conduction time (CT) and functional refractory period (FRP) of the A-V conduction system were studied in these dogs for comparison with those of control dogs. In the hyperthyroid group, A-V CT and FRP were markedly shortened, and the frequency at which the A-V conduction system can transmit rapid atrial impulses was significantly increased. The opposite changes were observed in the hypothyroid group. A-V CT and FRP decreased in the control and hyperthyroid groups during infusion of epinephrine at a rate of 1 mcg. per kilogram per minute, and these changes were comparable in both groups in terms of per cent changes. The results indicate that thyroid hormone markedly facilitates the impulse transmission through the A-V conduction system, and the action appears to be direct and independent of the sympathetic activity. This action may explain extremely rapid ventricular responses and increased digitalis requirements seen in thyrotoxic patients with atrial fibrillation.

Facilitation of A-V nodal reciprocation by procainamide*

Procainamide is known to depress conduction through the A-V node, and this property may facilitate the development of ventricular reciprocal beats or echoes. The occurrence of ventricular reciprocal beats was studied in 20 open-chest dogs before and after the administration of procainamide. While the ventricle was paced by basic stimuli, early ventricular premature beats were introduced at various coupling intervals to induce ventricular echoes. When ventricular echoes could be induced in a given heart, there was a continuous range of coupling intervals (or echo zone) within which ventricular echoes occurred. In the control state, no echo occurred in eight dogs and the echoes developed in 12 dogs with the mean echo zone of 38.3 msec. The effect of procainamide was studied at its therapeutic blood levels about 25 minutes after an intravenous injection of the drug in a dose of 10 mg. per kilogram. Of the first group of eight dogs, in which no echo occurred in the control state, four dogs developed ventricular echoes after the administration of procainamide with the mean echo zone of 29.3 msec. for the group. Of the second group of 12 dogs, in which ventricular echoes were induced in the control state, the administration of procainamide increased the echo zone in 10 dogs with the mean echo zone of 67.8 msec. for the group. Ventricular reciprocal beats were often sustained to produce short runs of supraventricular tachycardia in five dogs after the administration of procainamide. The results demonstrated a potentially deleterious effect of procainamide in facilitating the inducation of A-V nodal reciprocation by closely coupled ventricular premature beats.

Ventricular tachyarrhythmias induced by premature beats during acute coronary occlusion

Summary Ventricular tachyarrhythmias were induced in the ventricle during acute coronary occlusion by initiating closely coupled premature beats in the normal or ischemic areas. Acute coronary occlusion produced an initial decrease in the refractory period and conduction time in the affected area within about 3 min. of the start of coronary occlusion, followed by a subsequent increase in these parameters. Ventricular premature beats of the shortest coupling intervals could be initiated in the ischemic area during the initial phase of acute coronary occlusion when the refractory period was shortest, and these premature beats, in turn, induced ventricular tachyarrhythmias with an average time of 3 min 6 sec after the start of coronary occlusion. When the refractory period was subsequently increased in the ischemic area, ventricular premature beats of the shortest coupling intervals could be initiated in the normal area and these premature beats resulted in ventricular tachyarrhythmias with an average time of 7 min 10 sec after the start of coronary occlusion. The results indicate that ventricular premature beats initiated in the ischemic area are more likely to induce the tachyarrhythmias in the initial phase of acute coronary occlusion, while the premature beats initiated in the normal area are more likely to lead to ventricular tachyarrhythmias in the later stages of acute coronary occlusion.

Effect of ventricular premature beats on idioventricular pacemaker activity

Abstract The effect of ventricular premature beats on idioventricular pacemaker activity was studied in open-chest dog hearts with a surgically induced block in the His bundle. While the ventricle was paced by basic stimuli at a given rate, the pacing was interrupted for about 2.5 seconds following every twelfth basic beat (V 1 ) in order to obtain the interval between V 1 and the first escape beat (V e ) or the basic escape interval (V 1 V e ). Ventricular premature beats (V 2 ) were then introduced at various coupling intervals (V 1 V 2 ) and the effect of these premature beats on the postextrasystolic escape interval (V 1 V e ) was observed. The plot of V 2 V e against V 1 V 2 intervals showed that the V 2 V e interval was shortest at shorter V 1 V 2 intervals, and it increased gradually with the increase in V 1 V 2 intervals. The V 2 V e intervals at shorter coupling intervals were much shorter than the basic escape interval (V 1 V e ), indicating enhanced automaticity after early premature beats. The V 2 V e at longer coupling intervals were much longer than the basic escape intervals, indicating suppressed automaticity after late premature beats. The similar response to ventricular premature beats was noted during spontaneous idioventricular rhythm. The suppression was more pronounced at faster pacing rates and following two successive premature beats, probably due to the phenomenon of overdrive suppression. The same phenomena of altered automaticity after premature beats could be observed under the influence of ouabain, epinephrine, lidocaine, and propranolol, although these agents either decreased or increased the average escape intervals. The results may explain the clinically observed alteration of the idioventricular pacemaker rate following ventricular premature beats.